Finding. A biofilm amyloid can fire caspase-11 in dendritic cells and release IL-1β without killing the cell and without sending gasdermin D to mitochondria. Mintri, Fitzgerald, Gallucci and colleagues show that curli from Enterobacteriaceae biofilms is enough to prime (TLR2 and TLR4) and to activate the non-canonical inflammasome. Caspase-11 binds it. NLRP3 engages. IL-1β matures. The cell does not pyroptose. Mature gasdermin D makes a limited oligomer at the plasma membrane, skips mitochondria, and does not hand the ending to NINJ1. Those living DCs migrate more to draining lymph nodes. Whole curli-containing biofilms do the same non-lytic IL-1β trick.
Why this paper matters
This site has already filed gasdermins that pore mitochondria. The contrast class is now here: a natural biofilm ligand that keeps GSDMD off the organelle so the DC can stay a messenger. If you model inflammasome-mitochondria crosstalk, curli hyperactivation is the negative-control ligand.
It is also a host-biofilm paper. Chronic infection immunology has been short a named caspase-11 amyloid.
What they actually measured
Binding, priming, IL-1β, death (absent), GSDMD localization, NINJ1, in vivo migration, biofilms versus purified curli. No OCR.
How to read the score
Low 70s on a mitochondria rubric: the organelle is where GSDMD is not. Confidence is high for that negative.
Caveats
No bioenergetics. Migration is not a full adaptive-immunity study. Do not treat all amyloids as caspase-11 ligands.
What to do with it
If you stain GSDMD after inflammasome activation, add a mitochondrial mask and a curli arm. Pair this brief with the GSDME inner-membrane paper already in the corpus. Do not write a curli vaccine from this brief.